Losartan, enalapril and their combination on the prevention of left ventricular remodeling after AMI in rats
Yang Yuejin, Pei Zhang, Ying-mao Ruan
Abstract
Yang Yuejin, Pei Zhang, Ying-mao Ruan
Abstract
Objective To compare the effects of losartan, enalapril and their combination on the prevention of left ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in rats. Methods AMI was produced in female SD rats by ligating the left coronary artery. Forty eight hours after the procedure, the 83 surviving rats were randomly divided into four groups:(1) AMI controls, (2) losartan(3 mg·kg -1 ·d -1 ), (3) enalapril (1 mg·kg -1 ·d -1 ),and (4) concomitant losartan and enalapril (3 mg·kg -1 ·d -1 and 1 mg·kg -1 ·d -1 ) groups; and (5) sham operated group and (6) normal group were selected randomly to serve as non infarction controls. Losartan and enalapril were delivered by direct gastric gavage. After 4 weeks of medical therapy, hemodynamic studies were performed in each group, and the rat hearts were then fixed with 10% formalin, and pathologic analysis was performed. Complete experimental data obtained in 56 rats were analyzed, comprising of ① AMI controls ( n =11), ② losartan group ( n =10), ③ enalapril group ( n =10), ④ concomitant losartan and enalapril group( n =11), ⑤ sham operated group ( n =6) and ⑥ normal controls ( n =8). Results There were no significant differences among the four AMI groups in MI size (41.7%-43.4%, all P 0.05). Compared with sham operated rats, the left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), long and short axis length (L and D), as well as LV absolute and relative weight (LVAW and LVRW) in the AMI group were all significantly increased ( P 0.05-0.001), indicating that LVRM occurred after AMI. The maximum left ventricular pressure rising and dropping rates (±dp/dt) and their corrected values were significantly reduced in the AMI group (all P 0.001). Compared with the AMI group, LVEDP, LVV, LVAW and LVRW were all significantly decreased in all three treatment groups ( P 0.05-0.001). The corrected ±dp/dt was significantly enhanced in all three treatment groups ( P 0.05-0.001) except the corrected -dp/dt of the losartan group ( P 0.05). There were no significant differences in the above mentioned indices among the three treatment groups (all P 0.05). Conclusions Both losartan and enalapril can prevent LVRM after AMI in the rat and improve LV function with equivalent effects. There is no additive effect when the two drugs were used in combination.
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Objective To compare the effects of losartan, enalapril and their combination on the prevention of left ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in rats. Methods AMI was produced in female SD rats by ligating the left coronary artery. Forty eight hours after the procedure, the 83 surviving rats were randomly divided into four groups:(1) AMI controls, (2) losartan(3 mg·kg -1 ·d -1 ), (3) enalapril (1 mg·kg -1 ·d -1 ),and (4) concomitant losartan and enalapril (3 mg·kg -1 ·d -1 and 1 mg·kg -1 ·d -1 ) groups; and (5) sham operated group and (6) normal group were selected randomly to serve as non infarction controls. Losartan and enalapril were delivered by direct gastric gavage. After 4 weeks of medical therapy, hemodynamic studies were performed in each group, and the rat hearts were then fixed with 10% formalin, and pathologic analysis was performed. Complete experimental data obtained in 56 rats were analyzed, comprising of ① AMI controls ( n =11), ② losartan group ( n =10), ③ enalapril group ( n =10), ④ concomitant losartan and enalapril group( n =11), ⑤ sham operated group ( n =6) and ⑥ normal controls ( n =8). Results There were no significant differences among the four AMI groups in MI size (41.7%-43.4%, all P 0.05). Compared with sham operated rats, the left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), long and short axis length (L and D), as well as LV absolute and relative weight (LVAW and LVRW) in the AMI group were all significantly increased ( P 0.05-0.001), indicating that LVRM occurred after AMI. The maximum left ventricular pressure rising and dropping rates (±dp/dt) and their corrected values were significantly reduced in the AMI group (all P 0.001). Compared with the AMI group, LVEDP, LVV, LVAW and LVRW were all significantly decreased in all three treatment groups ( P 0.05-0.001). The corrected ±dp/dt was significantly enhanced in all three treatment groups ( P 0.05-0.001) except the corrected -dp/dt of the losartan group ( P 0.05). There were no significant differences in the above mentioned indices among the three treatment groups (all P 0.05). Conclusions Both losartan and enalapril can prevent LVRM after AMI in the rat and improve LV function with equivalent effects. There is no additive effect when the two drugs were used in combination.
Key concepts: Enalapril, Losartan, Medicine, Myocardial infarction, Cardiology, Ventricular remodeling, Internal medicine, Preload